Oxytocin does not acutely improve glucose tolerance in men with type 2 diabetes.

AIM: To assess oxytocin's acute glucoregulatory impact in men with type 2 diabetes in the context of our previous findings that oxytocin improves ß-cell responsivity in healthy men. METHODS: In a double-blind, crossover comparison, intranasal oxytocin (24 IU) and placebo, respectively, were administered to 25 fasted men with non-insulin-treated type 2 diabetes (age ± standard error of the mean, 63.40 ± 1.36 years; body mass index, 27.77 ± 0.66 kg/m2; HbA1c, 6.86% ± 0.08%; Homeostatic Model Assessment of Insulin Resistance (HOMA-IR, 3.44 ± 0.39) 60 minutes before an oral glucose tolerance test (oGTT). Key outcomes were compared with previous results in men with normal weight or obesity. RESULTS: Oxytocin compared with placebo increased plasma oxytocin concentrations and reduced the heart rate, but did not alter glucose metabolism in the 3 hours after oGTT onset (area under the curve, glucose, 2240 ± 80.5 vs. 2190 ± 69.5 mmol/L × min; insulin, 45 663 ± 4538 vs. 44 343 ± 4269 pmol/L × min; C-peptide, 235 ± 5.1 vs. 231 ± 15.9 nmol/L × min). CONCLUSIONS: This outcome contrasts with the oxytocin-induced attenuation of early postprandial glucose excursions in normal-weight individuals, but is in line with the absence of respective effects in men with obesity. We conclude that insulin resistance in type 2 diabetes is associated with decreased sensitivity to the acute glucoregulatory effect of oxytocin in male individuals.

The 'Behavioral Balance Model': A new perspective on the aetiology and therapy of obesity.

Obesity is a debilitating disease of global proportions that necessitates refined, concept-driven therapeutic approaches. Policy makers, the public and even health care professionals, but also individuals with obesity harbour many misconceptions regarding this disease, which leads to prejudice, negative attitudes, stigmatization, discrimination, self-blame, and failure to provide and finance adequate medical care. Decades of intensive, successful scientific research on obesity have only had a very limited effect on this predicament. We propose a science-based, easy-to-understand conceptual model that synthesizes the complex pathogenesis of obesity including biological, psychological, social, economic and environmental aspects with the aim to explain and communicate better the nature of obesity and currently available therapeutic modalities. According to our integrative 'Behavioral Balance Model', 'top-down cognitive control' strategies are implemented (often with limited success) to counterbalance the increased 'bottom-up drive' to gain weight, which is triggered by biological, psycho-social and environmental mechanisms in people with obesity. Besides offering a deeper understanding of obesity, the model also highlights why there is a strong need for multimodal therapeutic approaches that may not only increase top-down control but also reduce a pathologically increased bottom-up drive.

Late, but Not Early, Night Sleep Loss Compromises Neuroendocrine Appetite Regulation and the Desire for Food.

OBJECTIVE: There is evidence that reduced sleep duration increases hunger, appetite, and food intake, leading to metabolic diseases, such as type 2 diabetes and obesity. However, the impact of sleep timing, irrespective of its duration and on the regulation of hunger and appetite, is less clear. We aimed to evaluate the impact of sleep loss during the late vs. early part of the night on the regulation of hunger, appetite, and desire for food. METHODS: Fifteen normal-weight ([mean ± SEM] body-mass index: 23.3 ± 0.4 kg/m2) healthy men were studied in a randomized, balanced, crossover design, including two conditions of sleep loss, i.e., 4 h sleep during the first night-half ('late-night sleep loss'), 4 h sleep during the second night-half ('early-night sleep loss'), and a control condition with 8h sleep ('regular sleep'), respectively. Feelings of hunger and appetite were assessed through visual analogue scales, and plasma ghrelin and leptin were measured from blood samples taken before, during, and after night-time sleep. RESULTS: Ghrelin and feelings of hunger and appetite, as well as the desire for food, were increased after 'late-night sleep loss', but not 'early-night sleep loss', whereas leptin remained unaffected by the timing of sleep loss. CONCLUSIONS: Our data indicate that timing of sleep restriction modulates the effects of acute sleep loss on ghrelin and appetite regulation in healthy men. 'Late-night sleep loss' might be a risk factor for metabolic diseases, such as obesity and type 2 diabetes. Thereby, our findings highlight the metabolic relevance of chronobiological sleep timing.

A sweet spot for the sleeping brain: Linking human sleep physiology and glucoregulation.

Vallat et al.1 demonstrate a positive association between the coupling of slow oscillations and sleep spindles, neurophysiological markers of NREM sleep, and next-morning glucose homeostasis. Extended findings in an independent dataset raise intriguing questions about its directionality and consistency.

Vagus nerve stimulation increases stomach-brain coupling via a vagal afferent pathway.

BACKGROUND: Maintaining energy homeostasis is vital and supported by vagal signaling between digestive organs and the brain. Previous research has established a gastric network in the brain that is phase synchronized with the rhythm of the stomach, but tools to perturb its function were lacking. OBJECTIVE: To evaluate whether stomach-brain coupling can be acutely increased by non-invasively stimulating vagal afferent projections to the brain. METHODS: Using a single-blind randomized crossover design, we investigated the effect of acute right-sided transcutaneous auricular vagus nerve stimulation (taVNS) versus sham stimulation on stomach-brain coupling. RESULTS: In line with preclinical research, taVNS increased stomach-brain coupling in the nucleus of the solitary tract (NTS) and the midbrain while boosting coupling across the brain. Crucially, in the cortex, taVNS-induced changes in coupling occurred primarily in transmodal regions and were associated with changes in hunger ratings as indicators of the subjective metabolic state. CONCLUSIONS: taVNS increases stomach-brain coupling via an NTS-midbrain pathway that signals gut-induced reward, indicating that communication between the brain and the body is effectively modulated by vago-vagal signaling. Such insights may help us better understand the role of vagal afferents in orchestrating the recruitment of the gastric network which could pave the way for novel neuromodulatory treatments.

OXTR DNA methylation differentiates men on the obesity spectrum with and without binge eating disorder.

BACKGROUND: The neuropeptide oxytocin (OXT) plays a role in the regulation of eating behavior and metabolism. OXT functioning is altered in patients with eating and weight disorders, and a variant of the oxytocin receptor gene (OXTR) has been associated with impulsive eating behavior as it is seen in patients with binge eating disorder (BED). Gene × environment interactions could play a role in BED. One mechanism mediating this interaction is the epigenetic alteration of gene expression. We therefore investigated if DNA methylation of the OXTR differs between individuals with obesity depending on a comorbid BED. We analyzed DNA methylation of the OXTR in peripheral blood of 227 individuals on the obesity spectrum (mean age: 40.3 ± 13.1 yrs; mean BMI: 38.6 ± 7.3 kg/m2), 130 of which were diagnosed with BED. RESULTS: There were no overall differences in OXTR methylation between participants with and those without BED (p > 0.05), while both subgroups were comparable regarding age and body mass index (BMI), but significantly differed in sex distribution (p = 0.035). We found no relationship between mean DNA methylation and BMI or self-reported eating disorder (ED) pathology. Analyzing potential sex differences revealed a significantly lower OXTR DNA methylation in male participants with BED as compared to those without BED (p = 0.017). No such difference was found in the female subsample (p > 0.05). CONCLUSIONS: Clinically significant binge eating pathology might be associated with lower OXTR DNA methylation exclusively in males. The differential DNA methylation of OXTR in males with BED supports the view that BED represents a phenotype within the obesity spectrum that is characterized by specific vulnerability factors. A better understanding of the epigenetic underpinnings of the OXT system might contribute to the refinement of OXT administration approaches as potential interventions in eating and weight disorders.

Sleep deprivation prevents counterregulatory adaptation to recurrent hypoglycaemia.

AIMS/HYPOTHESIS: Attenuated counterregulation after recurrent hypoglycaemia is a major complication of diabetes treatment. As there is previous evidence for the relevance of sleep in metabolic control, we assessed the acute contribution of sleep to the counterregulatory adaptation to recurrent hypoglycaemia. METHODS: Within a balanced crossover design, 15 healthy, normal-weight male participants aged 18-35 years underwent three hyperinsulinaemic-hypoglycaemic clamps with a glucose nadir of 2.5 mmol/l, under two experimental conditions, sleep and sleep deprivation. Participants were exposed to two hypoglycaemic episodes, followed by a third hypoglycaemic clamp after one night of regular 8 h sleep vs sleep deprivation. The counterregulatory response of relevant hormones (glucagon, growth hormone [GH], ACTH, cortisol, adrenaline [epinephrine] and noradrenaline [norepinephrine]) was measured, and autonomic and neuroglycopenic symptoms were assessed. RESULTS: Sleep deprivation compared with sleep dampened the adaptation to recurrent hypoglycaemia for adrenaline (p=0.004), and this pattern also emerged in an overall analysis including adrenaline, GH and glucagon (p=0.064). After regular sleep, the counterregulatory responses of adrenaline (p=0.005), GH (p=0.029) and glucagon (p=0.009) were attenuated during the 3rd clamp compared with the 1st clamp, but were preserved after sleep deprivation (all p>0.225). Neuroglycopenic and autonomic symptoms during the 3rd clamp compared with the 1st clamp were likewise reduced after sleep (p=0.005 and p=0.019, respectively). In sleep deprivation, neuroglycopenic symptoms increased (p=0.014) and autonomic symptoms were unchanged (p=0.859). CONCLUSIONS/INTERPRETATION: The counterregulatory adaptation to recurrent hypoglycaemia is compromised by sleep deprivation between hypoglycaemic episodes, indicating that sleep is essential for the formation of a neurometabolic memory, and may be a potential target of interventions to treat hypoglycaemia unawareness syndrome.

The effect of intranasal insulin on appetite and mood in women with and without obesity: an experimental medicine study.

BACKGROUND/OBJECTIVES: Intranasal (IN) administration of insulin decreases appetite in humans, but the underlying mechanisms are unclear, and it is unknown whether IN insulin affects the food intake of women with obesity. SUBJECTS/METHODS: In a double-blind, placebo-controlled, crossover design, participants (35 lean women and 17 women with obesity) were randomized to receive 160 IU/1.6 mL of IN insulin or placebo in a counterbalanced order in the post prandial state. The effects of IN insulin on cookie intake, appetite, mood, food reward, cognition and neural activity were assessed. RESULTS: IN insulin in the post prandial state reduced cookie intake, appetite and food reward relative to placebo and these effects were more pronounced for women with obesity compared with lean women. IN insulin also improved mood in women with obesity. In both BMI groups, IN insulin increased neural activity in the insula when viewing food pictures. IN insulin did not affect cognitive function. CONCLUSIONS: These results suggest that IN insulin decreases palatable food intake when satiated by reducing food reward and that women with obesity may be more sensitive to this effect than lean women. Further investigation of the therapeutic potential of IN insulin for weight management in women with obesity is warranted.

Distinct and Convergent Beneficial Effects of Estrogen and Insulin on Cognitive Function in Healthy Young Men.

CONTEXT: Systematic investigations into the cognitive impact of estradiol and insulin in male individuals are sparse, and it is unclear whether the 2 hormones interact to benefit specific cognitive functions in humans. OBJECTIVE: We investigated the acute effect of estradiol and insulin and of their combined administration on divergent (creative) and convergent (arithmetical) thinking as well as short-term and working verbal memory in healthy young men. METHODS: According to a 2 × 2 design, 2 groups of men (each n = 16) received a 3-day transdermal estradiol (100 µg/24 h) or placebo pretreatment and on 2 separate mornings were intranasally administered 160 IU regular human insulin and, respectively, placebo before completing a battery of cognitive tests; we also determined relevant blood parameters. RESULTS: Estrogen compared with placebo treatment induced a 3.5-fold increase in serum estradiol and suppressed serum testosterone concentrations by 70%. Estrogen in comparison to placebo improved creative performance, that is, verbal fluency and flexibility, but not arithmetical thinking, as well as verbal short-term memory, but not visuospatial memory. The combination of estrogen and insulin enhanced recognition discriminability at delayed verbal memory recall; insulin alone remained without effect. CONCLUSION: Estrogen specifically enhances core aspects of creativity and verbal memory in young male individuals; delayed recognition memory benefits from the combined administration of estradiol and insulin. Our results indicate that insulin's acute cognitive impact in young men is limited and not robustly potentiated by estradiol. Estradiol per se exerts a beneficial acute effect on creative and verbal performance in healthy young men.

Predictors of real-time fMRI neurofeedback performance and improvement - A machine learning mega-analysis.

Real-time fMRI neurofeedback is an increasingly popular neuroimaging technique that allows an individual to gain control over his/her own brain signals, which can lead to improvements in behavior in healthy participants as well as to improvements of clinical symptoms in patient populations. However, a considerably large ratio of participants undergoing neurofeedback training do not learn to control their own brain signals and, consequently, do not benefit from neurofeedback interventions, which limits clinical efficacy of neurofeedback interventions. As neurofeedback success varies between studies and participants, it is important to identify factors that might influence neurofeedback success. Here, for the first time, we employed a big data machine learning approach to investigate the influence of 20 different design-specific (e.g. activity vs. connectivity feedback), region of interest-specific (e.g. cortical vs. subcortical) and subject-specific factors (e.g. age) on neurofeedback performance and improvement in 608 participants from 28 independent experiments. With a classification accuracy of 60% (considerably different from chance level), we identified two factors that significantly influenced neurofeedback performance: Both the inclusion of a pre-training no-feedback run before neurofeedback training and neurofeedback training of patients as compared to healthy participants were associated with better neurofeedback performance. The positive effect of pre-training no-feedback runs on neurofeedback performance might be due to the familiarization of participants with the neurofeedback setup and the mental imagery task before neurofeedback training runs. Better performance of patients as compared to healthy participants might be driven by higher motivation of patients, higher ranges for the regulation of dysfunctional brain signals, or a more extensive piloting of clinical experimental paradigms. Due to the large heterogeneity of our dataset, these findings likely generalize across neurofeedback studies, thus providing guidance for designing more efficient neurofeedback studies specifically for improving clinical neurofeedback-based interventions. To facilitate the development of data-driven recommendations for specific design details and subpopulations the field would benefit from stronger engagement in open science research practices and data sharing.

Body composition in term offspring after maternal gestational diabetes does not predict postnatal hypoglycemia.

BACKGROUND: Offspring of mothers with gestational diabetes mellitus (GDM) have an increased risk of neonatal complications like birth trauma due to macrosomia or postnatal hypoglycemia, as well as long-term metabolic sequelae. Neonatal body composition may be a sensitive marker of metabolic effects on the fetus caused by suboptimal glycemic control during pregnancy. OBJECTIVE: To determine body composition in offspring of mothers with GDM compared to a reference cohort of healthy term neonates and to assess whether increased body fat would be associated with postnatal hypoglycemia. METHODS: This prospective, observational, cross-sectional study included 311 full-term, singleton infants born between June 2014 and July 2015. Body composition was measured within 96 h of birth using air displacement plethysmography. Results are indicated as median (1st Quartile - 3rd Quartile). RESULTS: Of 311 infants, 40 (12.9%) were born to mothers with GDM. Birth weight standard deviation scores (SDS) (0.24 vs. - 0.07, p = 0.04), fat mass (370 g vs. 333 g, p = 0.02) as well as fat mass/total body mass (BF%; 11.4% vs. 10.8%, p = 0.03) were significantly higher in infants following maternal GDM than in controls. In GDM offspring, anthropometric parameters, fat mass or BF% did not differ between infants with or without postnatal hypoglycemia. In this cohort, SDS for birth weight, fat mass, fat free mass, BF% or postnatal hypoglycemia were not associated with maternal blood glucose levels measured at an oral glucose tolerance test. CONCLUSIONS: SDS for birth weight, neonatal fat mass, and BF% were significantly higher in newborns following maternal GDM. In these infants born to mothers with GDM, body composition did not differ between those with or without postnatal hypoglycemia.

Intranasal insulin.

The intranasal (IN) route enables the delivery of insulin to the central nervous system in the relative absence of systemic uptake and related peripheral side effects. Intranasally administered insulin is assumed to travel along olfactory and adjacent pathways and has been shown to rapidly accumulate in cerebrospinal fluid, indicating efficient transport to the brain. Two decades of studies in healthy humans and patients have demonstrated that IN insulin exerts functional effects on metabolism, such as reductions in food intake and body weight and improvements of glucose homeostasis, as well as cognition, ie, enhancements of memory performance both in healthy individuals and patients with mild cognitive impairment or Alzheimer's disease; these studies moreover indicate a favourable safety profile of the acute and repeated use of IN insulin. Emerging findings suggest that IN insulin also modulates neuroendocrine activity, sleep-related mechanisms, sensory perception and mood. Some, but not all studies point to sex differences in the response to IN insulin that need to be further investigated along with the impact of age. "Brain insulin resistance" is an evolving concept that posits impairments in central nervous insulin signalling as a pathophysiological factor in metabolic and cognitive disorders such as obesity, type 2 diabetes and Alzheimer's disease, and, notably, a target of interventions that rely on IN insulin. Still, the negative outcomes of longer-term IN insulin trials in individuals with obesity or Alzheimer's disease highlight the need for conceptual as well as methodological advances to translate the promising results of proof-of-concept experiments and pilot clinical trials into the successful clinical application of IN insulin.

Intranasal Insulin for Alzheimer's Disease.

Brain insulin signaling contributes to memory function and might be a viable target in the prevention and treatment of memory impairments including Alzheimer's disease. This short narrative review explores the potential of central nervous system (CNS) insulin administration via the intranasal pathway to improve memory performance in health and disease, with a focus on the most recent results. Proof-of-concept studies and (pilot) clinical trials in individuals with mild cognitive impairment or Alzheimer's disease indicate that acute and prolonged intranasal insulin administration enhances memory performance, and suggest that brain insulin resistance is a pathophysiological factor in Alzheimer's disease with or without concomitant metabolic dysfunction. Intranasally administered insulin is assumed to trigger improvements in synaptic plasticity and regional glucose uptake as well as alleviations of Alzheimer's disease neuropathology; additional contributions of changes in hypothalamus-pituitary-adrenocortical axis activity and sleep-related mechanisms are discussed. While intranasal insulin delivery has been conclusively demonstrated to be effective and safe, the recent outcomes of large-scale clinical studies underline the need for further investigations, which might also yield new insights into sex differences in the response to intranasal insulin and contribute to the optimization of delivery devices to grasp the full potential of intranasal insulin for Alzheimer's disease.

Association Between Objectively Assessed Sleep and Depressive Symptoms During Pregnancy and Post-partum.

INTRODUCTION: Sleep problems are common in pregnancy but many studies have relied only on self-reported sleep measures. We studied the association between objectively measured sleep and peripartum depressive symptoms in pregnant women. MATERIAL AND METHODS: Sleep was assessed using Actiwatch accelerometers in a sample of 163 pregnant women in the late first (weeks 11-15) or early second trimester (weeks 16-19). Depressive symptoms were assessed in gestational weeks 17, 32 and at 6 weeks post-partum using the Edinburgh Postnatal Depression Scale (EPDS). Multiple linear regression and logistic regression analyses, adjusting for age, BMI, pre-pregnancy smoking, ongoing mental health problems, trimester and season of sleep assessment were carried out to test the association between sleep and depression. Sleep was measured by total sleep time and sleep efficiency, whereas depression was indicated by depressive symptoms and depression caseness. Results are presented as unstandardized beta (B) coefficients or adjusted odds ratios (AOR) and 95% confidence intervals (CI). RESULTS: Total sleep time ranged from 3 to 9 h (mean 7.1, SD 0.9) and average sleep efficiency was 83% (SD 6.0). Women with the shortest total sleep time, i.e., in the lowest quartile (<6.66 h), reported higher depressive symptoms during pregnancy (week 17, B = 2.13, 95% CI 0.30-3.96; week 32, B = 1.70, 95% CI 0.03-3.37) but not post-partum. Their probability to screen positive for depression in gestational week 17 was increased more than 3-fold (AOR = 3.46, 95% CI 1.07-11.51) but unchanged with regards to gestational week 32 or 6 weeks post-partum. Sleep efficiency was not associated with depressive symptoms at any stage of pregnancy or post-partum. DISCUSSION: In one of the few studies to use objective sleep measures to date, mental health of pregnant women appeared to be affected by shortened sleep, with total sleep time being negatively associated with depressive symptoms in the early second and third trimester. This finding highlights the relevance of identifying and treating sleep impairments in pregnant women early during antenatal care to reduce the risk of concomitant depression.

Short-term high-fat feeding induces a reversible net decrease in synaptic AMPA receptors in the hypothalamus.

Dietary obesity compromises brain function, but the effects of high-fat food on synaptic transmission in hypothalamic networks, as well as their potential reversibility, are yet to be fully characterized. We investigated the impact of high-fat feeding on a hallmark of synaptic plasticity, i.e., the expression of glutamatergic α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors (AMPARs) that contain the subunits GluA1 and GluA2, in hypothalamic and cortical synaptoneurosomes of male rats. In the main experiment (experiment 1), three days, but not one day of high-fat diet (HFD) decreased the levels of AMPAR GluA1 and GluA2 subunits, as well as GluA1 phosphorylation at Ser845, in hypothalamus but not cortex. In experiment 2, we compared the effects of the three-day HFD with those a three-day HFD followed by four recovery days of normal chow. This experiment corroborated the suppressive effect of high-fat feeding on hypothalamic but not cortical AMPAR GluA1, GluA2, and GluA1 phosphorylation at Ser845, and indicated that the effects are reversed by normal-chow feeding. High-fat feeding generally increased energy intake, body weight, and serum concentrations of insulin, leptin, free fatty acids, and corticosterone; only the three-day HFD increased wakefulness assessed via video analysis. Results indicate a reversible down-regulation of hypothalamic glutamatergic synaptic strength in response to short-term high-fat feeding. Preceding the manifestation of obesity, this rapid change in glutamatergic neurotransmission may underlie counter-regulatory efforts to prevent excess body weight gain, and therefore, represent a new target of interventions to improve metabolic control.

Pregnant women do not display impaired memory formation across one night of sleep.

Forgetfulness is a common complaint of pregnant women, who also often report impaired nocturnal sleep. Considering sleep's well-known beneficial role in consolidating newly encoded memory content, we hypothesized that pregnant women would display detrimental changes in objective sleep measures and associated memory deficits. We compared the consolidation of declarative as well as procedural memory across sleep in 21 healthy, third-trimester pregnant women versus 20 matched non-pregnant controls. Subjects encoded and were tested on visuospatial and procedural memory tasks before and after, respectively, a night of sleep spent at home. The emergence of gist-based memories was tested with the Deese-Roediger-McDermott (DRM) paradigm. Sleep was polysomnographically recorded and subjective sleep quality was assessed with questionnaires. Although pregnant in comparison to non-pregnant women reported markedly impaired subjective sleep quality and efficiency, quantitative changes were limited to increases in wakefulness after sleep onset and reductions in rapid eye movement (REM) sleep. Retention of newly learned memory contents, which is believed to reflect sleep-associated memory consolidation, was comparable between groups, as was the formation of gist-based memories. The findings indicate that subjective deteriorations in sleep quality experienced by pregnant women are not necessarily linked to objective impairments. They raise the possibility that sufficient slow wave sleep towards the end of pregnancy allows for normal sleep-related memory consolidation. Although these results were obtained in a small number of pregnant women in very good health and should be corroborated in larger samples, they challenge the assumption of poor sleep and impaired memory as hallmarks of the "pregnancy brain".

Vagus nerve stimulation boosts the drive to work for rewards.

Interoceptive feedback transmitted via the vagus nerve plays a vital role in motivation by tuning actions according to physiological needs. Whereas vagus nerve stimulation (VNS) reinforces actions in animals, motivational effects elicited by VNS in humans are still largely elusive. Here, we applied non-invasive transcutaneous auricular VNS (taVNS) on the left or right ear while participants exerted effort to earn rewards using a randomized cross-over design (vs. sham). In line with preclinical studies, acute taVNS enhances invigoration of effort, and stimulation on the left side primarily facilitates invigoration for food rewards. In contrast, we do not find conclusive evidence that acute taVNS affects effort maintenance or wanting ratings. Collectively, our results suggest that taVNS enhances reward-seeking by boosting invigoration, not effort maintenance and that the stimulation side affects generalization beyond food reward. Thus, taVNS may enhance the pursuit of prospective rewards which may pave avenues to treat motivational deficiencies.

Visual food cues decrease blood glucose and glucoregulatory hormones following an oral glucose tolerance test in normal-weight and obese men.

Previous experiments of our group have demonstrated that preprandial processing of food cues attenuates postprandial blood glucose excursions. Here we systematically re-evaluated the glucose-lowering effect of visual food cues by submitting 40 healthy fasted men (20 normal-weight men, mean age 24.8 ± 3.7 years, BMI 21.9 ± 0.3 kg/m2; 20 obese men, 26.8 ± 4.2 years, 34.3 ± 1.3 kg/m2) to an oral glucose tolerance test (OGTT) following exposure to pictures of high-calorie food items versus neutral items. OGTT-related changes in blood concentrations of glucose and relevant glucoregulatory hormones including GLP-1 were assessed and analyzed according to the oral minimal model. Independent of body weight, food-cue compared to neutral stimulus presentation reduced postprandial concentrations of glucose (p = 0.041), insulin (p = 0.026) and C-peptide (p = 0.007); accordingly, oral minimal model analyses yielded a food-cue induced decrease of dynamic-phase insulin secretion (p = 0.036). We also observed a trend towards lower GLP-1 levels directly after food cue stimulation in both body weight groups (p = 0.057), as well as a trend towards decreased heart rate (p = 0.093) and significantly decreased diastolic blood pressure (p = 0.019). While we did not detect indicators of an early rise in insulin levels in terms of a 'cephalic phase insulin response', our findings support the assumption that preprandial processing of food cues exerts marked effect on postprandial glucose regulation, with possible contributions of changes in GLP-1. The mechanisms linking food cue exposure and glucoregulatory improvements should be investigated in greater detail, to potentially open new treatment options for metabolic dysfunctions.